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Wählen Sie konfigurierbare Panels & Premixed-Kits - ODER - Kits für die zelluläre Signaltransduktion & MAPmates™
Konfigurieren Sie Ihre MILLIPLEX® MAP-Kits und lassen sich den Preis anzeigen.
Konfigurierbare Panels & Premixed-Kits
Unser breites Angebot enthält Multiplex-Panels, für die Sie die Analyten auswählen können, die am besten für Ihre Anwendung geeignet sind. Unter einem separaten Register können Sie das Premixed-Cytokin-Format oder ein Singleplex-Kit wählen.
Kits für die zelluläre Signaltransduktion & MAPmates™
Wählen Sie gebrauchsfertige Kits zur Erforschung gesamter Signalwege oder Prozesse. Oder konfigurieren Sie Ihre eigenen Kits mit Singleplex MAPmates™.
Die folgenden MAPmates™ sollten nicht zusammen analysiert werden: -MAPmates™, die einen unterschiedlichen Assaypuffer erfordern. -Phosphospezifische und MAPmate™ Gesamtkombinationen wie Gesamt-GSK3β und Gesamt-GSK3β (Ser 9). -PanTyr und locusspezifische MAPmates™, z.B. Phospho-EGF-Rezeptor und Phospho-STAT1 (Tyr701). -Mehr als 1 Phospho-MAPmate™ für ein einziges Target (Akt, STAT3). -GAPDH und β-Tubulin können nicht mit Kits oder MAPmates™, die panTyr enthalten, analysiert werden.
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Custom Premix Selecting "Custom Premix" option means that all of the beads you have chosen will be premixed in manufacturing before the kit is sent to you.
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Gewähltes Kit
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96-Well Plate
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48-602MAG
Buffer Detection Kit for Magnetic Beads
1 Kit
Platzsparende Option Kunden, die mehrere Kits kaufen, können ihre Multiplex-Assaykomponenten in Kunststoffbeuteln anstelle von Packungen erhalten, um eine kompaktere Lagerung zu ermöglichen.
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AB3610
Sigma-AldrichAnti-Survivin Antibody
This Anti-Survivin Antibody is validated for use in WB, IP, IH for the detection of Survivin.
More>>This Anti-Survivin Antibody is validated for use in WB, IP, IH for the detection of Survivin. Less<<
Anti-Survivin Antibody: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
Apoptosis is triggered by a variety of stimuli, including members of the Tumor Necrosis Factor (TNF) family, and prevented by the inhibitor of apoptosis (IAP) proteins. IAP proteins form a conserved gene family that binds to and inhibits cell death proteases. One of these IAP proteins, Survivin/TIAP, interacts with the processed form of caspase-3 and has been shown to inhibit its proteolytic activity. Survivin/TIAP is predominantly expressed in tissues of embryos, transformed cell lines, and many human cancers and lymphomas.
This gene is a member of the inhibitor of apoptosis (IAP) gene family, which encode negative regulatory proteins that prevent apoptotic cell death. IAP family members usually contain multiple baculovirus IAP repeat (BIR) domains, but this gene encodes proteins with only a single BIR domain. The encoded proteins also lack a C-terminus RING finger domain. Gene expression is high during fetal development and in most tumors yet low in adult tissues. Antisense transcripts are involved in the regulation of this gene's expression. At least four transcript variants encoding distinct isoforms have been found for this gene, but the full-length natures of only three of them have been determined.
FUNCTION: SwissProt: O15392 # May play a role in neoplasia. May counteract a default induction of apoptosis in G2/M phase. Interacts with tubulin. Inhibitor of caspase-3 and caspase-7. Component of the chromosomal passenger complex (CPC), a complex that acts as a key regulator of mitosis. The CPC complex has essential functions at the centromere in ensuring correct chromosome alignment and segregation and is required for chromatin-induced microtubule stabilization and spindle assembly. Isoforms 2 and 3 do not appear to play vital roles in mitosis. Isoform 3 shows a marked reduction in its anti- apoptotic effects when compared with the displayed wild-type isoform. SIZE: 142 amino acids; 16390 Da SUBUNIT: Homodimer. When phosphorylated, interacts with HBXIP; the resulting complex binds pro-caspase-9, as well as active caspase- 9, but much less efficiently. Component of the CPC at least composed of BIRC5/survivin, CDCA8/borealin, INCENP and AURKB/Aurora-B. Interacts with EVI5. SUBCELLULAR LOCATION: Cytoplasm. Nucleus. Note=Localizes on chromosome arms and inner centromeres from prophase through metaphase and then transferring to the spindle midzone and midbody from anaphase through cytokinesis. Colocalizes with AURKB at mitotic chromosomes. TISSUE SPECIFICITY: Expressed only in fetal kidney and liver, and to lesser extent, lung and brain. Abundantly expressed in adenocarcinoma (lung, pancreas, colon, breast, and prostate) and in high-grade lymphomas. Also expressed in various renal cell carcinoma cell lines. DOMAIN: SwissProt: O15392 The BIR repeat is necessary and sufficient for HBXIP binding. SIMILARITY: Belongs to the IAP family. & Contains 1 BIR repeat.
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Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Maintain at -20°C for up to 6 months after date of receipt.
Inhibition of IL-6 expression in LNCaP prostate cancer cells by a combination of atorvastatin and celecoxib. Wang, H; Cui, XX; Goodin, S; Ding, N; Van Doren, J; Du, Z; Huang, MT; Liu, Y; Cheng, X; Dipaola, RS; Conney, AH; Zheng, X Oncology reports
31
835-41
2014
In the present study, we investigated the effect of a combination of atorvastatin and celecoxib on the formation of interleukin (IL)-6, a cytokine that is increased during the progression of LNCaP tumors from androgen dependence to androgen independence. Culturing LNCaP cells in androgen‑depleted (AD) medium increased the levels of IL-6 and survivin, and treatment of the cells in AD medium with a combination of atorvastatin and celecoxib strongly inhibited the increase in IL-6 and survivin which is one of the downstream targets of the IL-6 signaling pathway. Addition of recombinant IL-6 partially abrogated the combined effect of atorvastatin and celecoxib on apoptosis in LNCaP cells cultured in AD medium. In SCID mice, we found that the levels of IL-6 and survivin expression were increased when LNCaP tumors became androgen-independent. Treatment of the mice with atorvastatin or celecoxib alone caused decrease in the levels of IL-6 and survivin as LNCaP tumors became androgen-independent, but treatment of the mice with a combination of celecoxib and atorvastatin resulted in a much stronger inhibition in the increase in IL-6 and survivin expression. Our results indicate that decreases in IL-6 and survivin levels by atorvastatin and celecoxib administration are associated with increased apoptosis in LNCaP cells treated with this drug combination. Our in vivo studies indicate that the inhibitory effect of a combination of atorvastatin and celecoxib on the progression of androgen-dependent LNCaP xenograft tumors to androgen independence is associated with inhibition of the increase in IL-6 and survivin that occurs when androgen-dependent LNCaP prostate tumors become androgen-independent.
